Cupric Oxide Nanoparticles Induce Cellular Toxicity in Liver and Intestine Cell Lines

Purpose: The wide application of cupric oxide nanoparticles (copper (II) oxide, CuO-NPs) in various fields has increased exposure to the kind of active nanomaterials, which can cause negative effects on human and environment health. Although CuO-NPs were reported to be harmful to human, there is still a lack information related to their toxic potentials. In the present study, the toxic potentials of CuO-NPs were evaluated in the liver (HepG2 hepatocarcinoma) and intestine (Caco-2 colorectal adenocarcinoma) cells

Determination of Perflourooctanoic Acid Toxicity in a Human Hepatocarcinoma Cell Line

© Pure EarthBackground. Perfluorooctanoic acid (PFOA) is used in different industrial and commercial products. Research shows the presence of PFOA in home dusts, tap and surface water, and in biological samples. The International Agency for Research on Cancer (IARC) has classified PFOA as a possible carcinogen for humans. The liver is thought to be a target organ of PFOA accumulation and toxicity. Objective. Some studies have found toxic effects on the liver and related mechanisms; however, more studies are needed to better understand PFOA -induced hepatotoxicity. Methods. In the present study, a human hepatocarcinoma cell line was exposed to PFOA for 24 hours and cell viability, apoptosis, the oxidative system and immune response were evaluated. Results. While apoptosis was the main cell death pathway at low concentration (86.5%), the necrotic cell fraction increased with higher concentrations (46.7%). Significant changes in the reactive oxygen species (5.3-folds) glutathione (GSH) (1.7-folds) and catalase (CAT) (1.4-folds) levels were observed, as well as changes to interleukin-6 (≤1.8-fold) and interleukin-8 levels (35-40%). Conclusions. In light of the data, PFOA is potentially hepatotoxic through the investigated pathways. The results represent a background for future in vivo mechanistic studies. Competing Interests. The authors declare no competing financial interests

Nickel Oxide Nanoparticles Induce Oxidative DNA Damage and Apoptosis in Kidney Cell Line (NRK-52E)

Increasing use of nickel oxide (NiO) nanoparticles in different applications results in high occupational and environmental exposure to them. However, the effect of NiO nanoparticles on human health is still poorly documented. It was aimed to investigate the toxic potentials of NiO nanoparticles on NRK-52E kidney epithelial cells. The following assays were used: the nanoparticle characterization by transmission electron microscopy (TEM) and dynamic light scattering (DLS); the determination of cellular uptake and morphologic changes by TEM and inductively coupled plasma-mass spectrometry (ICP-MS); MTT and neutral red uptake (NRU) assays for cytotoxicity; comet assay for genotoxicity; the determination of malondialdehyde (MDA), 8-hydroxydeoxyguanosine (8-OHdG), protein carbonyl (PC) and glutathione (GSH) levels by enzyme-linked immune sorbent assays (ELISA) for the potential of oxidative damage; and Annexin V-FITC apoptosis detection assay with propidium iodide (PI) for apoptosis. The nanoparticles were taken up by the cells and induced dose-dependent DNA damage by comet assay and oxidative damage evidenced by increasing levels of MDA, 8-OHdG, PC and depletion of GSH. At >= 294.0 mu g/mL concentration, NiO nanoparticles caused 50% inhibition in cell viability by the cytotoxicity assays. Also, they showed apoptotic/necrotic effects on the cells as well as some morphological changes. We have indicated that their cellular damage effects should raise concern about the safety associated with their applications in consumer products

Cytotoxic, Genotoxic, and Apoptotic Effects of Nickel Oxide Nanoparticles in Intestinal Epithelial Cells

Objectives: The superior properties of nickel oxide-nanoparticles (NiO-NPs) have led to their wide use in various fields. However, there is little comprehensive knowledge about their toxicity, especially after oral exposure. The toxic effect of NiO-NPs of mean size 15.0 nm was investigated in Caco-2 (human intestinal epithelial) cells as no study has been performed on their intestinal toxicity

Assessment of perfluorooctanoic acid toxicity in pancreatic cells

Perfluorooctanoic acid (PFOA) was classified as a possible carcinogen for humans (Group 2B). The in vivo studies have reported that PFOA might lead to hepatic, testicular and pancreatic toxicities and cancers. However, its mechanisms in pancreatic tissue are still unclear and insufficiently discussed. Since inflammation is the most important mechanism leading to pancreatitis and ultimately cancer, we aimed to investigate the role of inflammation in PFOA-induced pancreatic toxicity. To this end, the effect of PFOA on cell viability, apoptosis, oxidative stress and inflammatory pathways, as well as levels of trypsin and chymotrypsin were assessed in the human pancreatic cell line (PANC-1). PFOA caused cell death in concentration dependent manner (IC50 195.6 mu M), apoptosis appears to be the major cell death pathway. A significant increase in trypsin and chymotrypsin levels was detected in PANC-1 cells. Oxidative stress parameters and gene expression level-related inflammation were significantly altered with PFOA exposure. These results indicate oxidative stress plays a role in PFOA-induced pancreatic toxicity and highlight the incidence of inflammation with PFOA exposure. However, this data is preliminary. Advanced in vivo and in vitro mechanistic studies should be conducted in order to better understand the inflammation-induced oxidative stress role in the toxicity of PFOA